Congestive Heart Failure (“CHF”), or simply “Heart Failure” is a progressive path found in many forms of heart disease. In general, it is a condition in which the heart is unable to pump blood at a rate sufficient for the proper supply of nutrients to metabolizing tissues. There are many specific disease states leading to CHF, but each typically results in the dilatation of the ventricles. Various etiologies for CHF are viral and ischemic and, of course, idiopathic. Myocardial injury and chronic volume overload generally are thought to cause this course of ventricular dilatation. The typical adaptation process undertaken by the stressed heart muscle is not achieved during CHF and, instead of gaining a stronger heart muscle, the heart instead gets larger as it attempts to adapt to its increased volume load.
Chronic pressure overload causes another response mechanism to develop. Specifically, hypertrophy of the heart muscle, entailing an increase both in the size of individual muscle cells and in overall muscle mass, begins to occur. Although this response helps the heart to overcome higher pressure, it has limitations and is associated with various structural and biochemical changes that have deleterious long term effects.
Additionally, system-wide vascular constriction occurs during the course of CHF. The constriction causes blood flow to be redistributed so that certain regions and systems have a reduced blood supply, e.g., skeletal muscle, kidneys, and skin. These regions do not produce significant amounts of vasodilating metabolites. In contrast, the brain and heart have high metabolic rates and produce a greater amount of vasodilators. Consequently, the latter organs receives a higher proportion of the restricted blood supply.
Therapy for CHF is staged. Correction of a reversible causative factors is the first line of offense. Treatment of bradyarrhythmias, perhaps by use of an artificial pacemaker or by provision of an appropriate drug such as digitalis, can help alleviate CHF. CHF that continues after correction of such reversible causes is often treated with a regime of salt restriction, vasodilators, diuretics, and the like. Bed rest to increase venous return to the heart and move fluid from the periphery is often helpful. As noted above, digitalis has been an important drug for increasing cardiac output in persons with specific types of CHF. It has been used for over 200 years. Other drugs used for treatment of CHF include beta-adrenergic agonists such as norepinephrine, epinephrine, and isoproterenol. Each stimulate cardiac beta-adrenergic receptors. Dopamine and dobutamine are also used. Various diuretics and vasodilators for variously dilating both veins and arteries are used, each for slightly different reasons based on the detected manifestation of the CHF in the heart.
Few interventional or surgical pathways for alleviation of CHF are currently widely practiced. Indeed, the only permanent treatment for CHF is a heart transplant.
One surgical procedure known as cardiomyoplasty is used for early stage CHF. In that procedure, a muscle taken from the shoulder (the latissimus dorsi) is wrapped around the heart. The added muscle is paced synchronously with the ventricular systole. This procedure is highly invasive requiring a sternotomy to access the heart. Some have suggested that the benefits of the procedure are due more to remodeling from the mere placement of the shoulder muscle around the heart rather than from a muscular assistance.
There are a variety of devices that may be applied to the heart for treatment of CHF. Patents owned by Abiomed (U.S. Pat. Nos. 6,224,540; 5,800,528; 5,643,172) generally show a girdle-like device situated to provide structure to a failing heart. U.S. Patents owned by Acorn Cardiovascular, Inc. (U.S. Pat. Nos. 6,241,654; 6,230,714; 6,193,648; 6,174,279; 6,169,922; 6,165,122; 6,165,121; 6,155,972; 6,126,590; 6,123,662; 6,085,754; 6,077,218; 5,702,343) show various devices, also for treatment of CHF, which typically include a mesh sock-like device placed around the myocardial wall. U.S. Patents to Myocor, Inc. (U.S. Pat. Nos. 6,264,602; 6,261,222; 6,260,552; 6,183,411; 6,165,120; 6,165,119; 6,162,168; 6,077,214; 6,059,715; 6,050,936; 6,045,497; 5,961,440) show devices for treatment of CHF generally using components that pierce the ventricular wall.
None of the documents mentioned above appears to suggest the devices and methods provided for herein.